Kruesi et al. (1987) evaluated the effect of sugar and aspartame
on 'aggression and activity' in preschool boys (ages 2 to 6 years) who were
identified as 'sensitive to sugar' by their parents. The study was a
double-blind cross-over challenge with aspartame (30 mg/kg bw), sucrose (1.75
g/kg bw), saccharin (amount not specified) and glucose (1.75 g/kg bw) to
sugar-responsive (children described as being sensitive to sugar; n = 14) and
age-matched control boys (n = 10). The sweeteners were given in a lemon-flavoured
drink each sweetener was given on two occasions; once in a laboratory
setting, and once 4 days later in a home setting. Children were scored for
'aggression and activity' by researchers during the laboratory playroom
challenge, and by their parents in the days following the challenge to detect
any delayed reaction, and during the home challenge. Washout periods of 5–7
days occurred between challenges.

Page 694 Column 1

Kruesi et al. (1987) evaluated the effect of sugar and aspartame
on aggression and activity in preschool boys (ages 2 to 6 years) who were
identified as sensitive to sugar or “sugar responders”. The study was a
double-blind cross-over challenge with aspartame (30 mg/kg bw), sucrose (1.75
g/kg bw), saccharin (amount not specified) and glucose (1.75 g/kg bw) to
sugar-responsive (n = 14) and age-matched control boys (n = 10). The
sweeteners were given in a lemon-flavored drink once in a laboratory setting,
and once 4 days later in a home setting. Children were scored for activity
and aggression by researchers during the laboratory playroom challenge and by
their parents in the days following to detect any delayed reaction, and
during the home challenge.Washout periods of 5–7 days occurred between
challenges.

3

2

3416 - 3426

In a randomised, double blind, and placebo-controlled crossover
study Shaywitz et al. (1994) assessed the effect of aspartame on behaviour
and cognitive function of children with attention deficit disorder. The dose
of aspartame was 34 mg/kg bw/day. The children (n = 15, 11 males, 4 females,
ages 5 to 13 years) were given capsules of either aspartame or placebo
(microcrystalline cellulose) each morning for a 2-week period. Parents were
instructed to provide an aspartame-free diet during the study. No effect was
found on cognitive, attentive or behavioural testing or on urinary levels of
neurotransmitters (noradrenaline, adrenaline, dopamine, homovanilic acid and
5-hydroxyindoleacetic acid), but plasma tyrosine and phenylalanine levels
were higher 2 hours after the aspartame treatment. Plasma tyrosine level
values were not provided. Plasma phenylalanine levels are only reported
graphically, and increased from approximately 60 μM at baseline to
approximately 85 μM two hours after aspartame dosing.

Page 694 Column 2

Shaywitz et al. (1994b) assessed the effect of aspartame on
behavior and cognitive function of children with attention deficit disorder
using a randomized, double blind, and placebo-controlled crossover study
design. The dose of aspartame was 34 mg/kg bw/day. Children (n = 15, 11
males, 4 females, ages 5 to 13 years) were given capsules of either aspartame
or placebo (microcrystalline cellulose) each morning for a 2-week period.
Parents were instructed to provide an aspartame-free diet during the study.
No effect was found on cognitive, attentive or behavioral testing or on
urinary levels of neurotransmitters (norepinephrine, epinephrine, dopamine,
HVA, and 5HIAA), although plasma tyrosine and phenylalanine levels were
higher 2 h after the aspartame treatment. Plasma phenylalanine levels were
reported graphically, and increased from approximately 6 μmol/dl at
baseline to about 8.5 μmol/dl 2 h after aspartame dosing.

2

3

3432 - 3436

A double-blind randomised crossover trial (Lapierre et al.,
1990) with 10 healthy adult volunteers (6 men, 4 women, ages 21–36 years)
evaluated the effect of a single dose of aspartame (15 mg/kg bw) or placebo
capsules on mood, cognitive function, and reaction time. No effect was
observed on any of the parameters measured (i.e. hunger, headache, memory,
reaction time, or cognition) during the study despite elevation of plasma
phenylalanine levels following consumption (data values not reported).

Page 695 Column 1

A double-blind randomized crossover trial with 10 healthy
volunteers (6 men, 4women, ages 21–36 years) evaluated the effect of a single
dose of aspartame (15 mg/kg bw) or placebo capsules on mood, cognitive
function, and reaction time. No effect was observed on hunger, headache,
memory, reaction time, or cognition during the study despite elevation of
plasma phenylalanine levels following consumption (data values not reported).
The percentage of total LNAA that was phenylalanine increased from approximately
11% to a peak of about 18 at the 2-h time point after dosing, but dropped to
normal after 8 h (Lapierre et al., 1990).

1

1

3443 -3444

Pivonka and Grunewald (1990) compared the effect of water, and
aspartame and sugar-containing beverages on mood in 120 young women and found
no effect on self-reported surveys of mood.

Page 695 Column 1

Pivonka and Grunewald (1990) compared the effect of water, and
aspartame- and sugar-containing beverages on mood in 120 young women and
found no effect on self-reported surveys of mood.

1

0

3446 -3457

The acute study (Stokes et al., 1991) involved 12 healthy
certified pilots (four females and eight males). The study was double-blinded
with each subject undertaking testing on 5 occasions, with at least 1 week
between treatments that were given in random order among the 12 participants.
Participants were tested for baseline values, then given placebo capsules,
aspartame (50 mg/kg bw), or ethyl alcohol (positive control, estimated dose
to raise plasma alcohol 0.1%), followed by a post-test with 3451 no treatment.
For all treatments, participants consumed orange juice with either a trace or
the test dose of alcohol, and capsules containing either placebo (dextrose)
or aspartame, all participants consumed a small carbohydrate meal prior to
treatments. Cognitive performance was tested using the SPARTANS cognitive
test battery (a sensitive test to detect changes in performance of complex
tasks required for aircraft operations). Cognitive impairment was detected in
several tasks following consumption of the low dose of alcohol but not
aspartame or placebo treatments.

Page 695 Column 1 and Column 2

The first study involved 12 healthy certified pilots (4 females
and 8 males). The study was double-blinded with each subject being tested 5
times, with at least 1 week between treatments given in random order among
the 12 participants. Participants were pretested for baseline values, then
given placebo capsules, aspartame (50 mg/kg bw), or ethyl alcohol (positive
control, estimated dose to raise blood alcohol 0.1%), followed by a posttest
with no treatment. For all treatments, participants consumed orange juice
with either a trace or the test dose of alcohol, and capsules with either
placebo (dextrose) or aspartame. Cognitive performancewas tested using the
SPARTANS cognitive test battery, which is a sensitive test to detect changes
in performance of complex tasks required for aircraft operations. As has been
discussed previously, concerns have been voiced regarding the possible
potentiation of the effects of aspartame by consumption concurrently with
carbohydrates. Therefore, all participants consumed a small carbohydrate meal
prior to treatments. Consumption of other foods, aspartame, and alcohol was
controlled prior to testing. Blood levels of amino acids were not measured.
Cognitive impairment was detected in several tasks following consumption of
the low dose of alcohol but not aspartame or placebo treatments (Stokes et
al., 1991).

3

4

EFSA actually made several edits to make the Ajinomoto-sponsored
review text more concise. Some sentences are still word-for-word (the exact
same). It must be so much easier to draft a long review when you can start
with an industry-funded review and make a few edits!

3458 - 3467

The follow up study (Stokes et al., 1994) was undertaken in 12
subjects (college students, sex not reported) received placebo capsules or
aspartame capsules (50 mg/kg bw/day) for 9 days, or an acute dose of ethyl
alcohol to achieve 0.1% blood ethanol levels as described above. All
participants received the placebo and ethanol treatments once and the
aspartame treatment twice with a 7-day period between treatments. On the last
day of treatment periods plasma phenylalanine levels averaged 59 μM
following placebo treatments and 121.5 μM following aspartame
consumption. Forty-seven task variables were measured and significant
differences between pre- and post-test results and aspartame treatment were
detected for three tasks. However, an improvement, rather than impairment, of
function was observed in participants following the aspartame treatments,
which the authors described as unexpected and attributed to chance.

Twelve subjects (college students, sex not defined) received
placebo capsules or aspartame capsules (50 mg/kg bw/day) for 9 days, or an
acute dose of ethyl alcohol to achieve 0.1% blood ethanol levels as described
earlier. All participants received the placebo and ethanol treatments once
and the aspartame treatment twice with a 7-day interval. Blood phenylalanine
and breath alcohol levels were measured. On the last day of treatment
periods, when subjects completed the cognitive testing, blood alcohol levels
were 0.0% during all treatments except following the alcohol treatment when
it averaged 0.09%. Plasma phenylalanine levels averaged 59.08 μmol
following placebo treatments and 121.5 μmol following aspartame
consumption. Forty-seven task variables were measured and significant
differences between pre- and post-test results and aspartame treatment were
detected for three tasks. However, unexpectedly, an improvement, rather than
impairment, of function was observed in participants following the aspartame
treatments.

1

4

When the EFSA was discussing these studies that do not measure
the effects on pilots of aspartame use over months and years, they forgot to
mention the Aspartame Pilot Hotline or the publications in aviation journals
about aspartame: The Aviation Consumer (1988), Aviation Medical Bulliten
(1988),
Pacific Flyer (1988), CAA General Aviation (1989), Aviation Safety Digest
(1989), General Aviation News (1989), Plane & Pilot (1990), Canadian
General Aviation News (1990), National Business Aircraft Association Digest
(NBAA Digest 1993), International Council of Air Shows (ICAS 1995), Pacific
Flyer (1995).U.S.
Air Force's magazine "Flying Safety" (1992) and the U.S. Navy's
magazine,
"Navy Physiology."

3468 - 3475

In a three-way crossover double-blind study a group of 48
healthy volunteers (24 men, 24 women, ages 18–34 years) received treatments
consisting of aspartame, sucrose and placebo administered for 20 days (Spiers
et al., 1998). Twenty-four participants received a high dose of aspartame (45
mg/kg bw/day) and the remaining received a low dose of aspartame (15 mg/kg
bw/day). Acute effects were evaluated on day 10 of each treatment, with
testing starting 90 min after consumption of test material; chronic effects
were evaluated on day 20. Plasma phenylalanine levels increased dose
dependently with aspartame consumption, but no cognitive, neurophysiologic
and behavioural effects were observed

Page 695 Column 2

Cognitive, neurophysiologic and behavioral effects of consuming
aspartame for 20 days were evaluated by Spiers et al. (1998) in a group of 48
healthy volunteers (24 men, 24 women, ages 18–34 years). This was a three-way
crossover doubleblind study with treatments consisting of aspartame, sucrose
and placebo. Twenty-four participants received a high dose of aspartame (45
mg/kg bw/day) and the remaining received 15 mg/kg bw/day. Acute effects were
evaluated on day 10 of each treatment arm, with testing starting 90 min after
consumption of test material. Chronic effects were evaluated on day 20.
Plasma phenylalanine levels increased dose-dependently with aspartame
consumption, but no other effects were observed.

2

2

I guess that EFSA was too busy copying and pasting to read the
study and see that the authors picked subjects who had used aspartame without
reacting. In the author's words: "In summary, we made a conscious effort
to preselect individuals who we felt would be unlikely to experience any
effect from chronic aspartame exposure." After months or years, even
these subjects will likely experience chronic aspartame poisoning. Please
see: http://www.holisticmed.com/aspartame/abuse/and
http://www.holisticmed.com/aspartame/aspfaq.html

3491 - 3492

Overall, the Panel concluded that the weight-of evidence
suggested that aspartame ingestion had no effect on behaviour or cognitive
function.

Page 696 Column 1

Overall, the weight of the evidence indicates that aspartame has
no effect on behavior or cognitive function.

A double-blind study was undertaken in children recently
diagnosed with generalised absence seizures or also called petit mal seizures
to ascertain whether aspartame would exacerbate the occurrence of such
seizures (Camfield et al., 1992). After eating breakfast of their own choice,
children (n = 10)drank orange juice
sweetened with either aspartame (40 mg/kg bw) or sucrose (1 g sucrose for
every 25 mg aspartame) to achieve similar sweetness.

Page 696 Column 1

Children who had been recently diagnosed with generalized
absence seizures were enrolled in a double-blind controlled study to
ascertain whether aspartame would exacerbate occurrence of absence seizures
(also called petite mal seizures) (Camfield et al., 1992). After eating their
own choice of breakfast, children (n = 10) drank orange juice sweetened with
either aspartame (40 mg/kg bw) or sucrose (1 g sucrose for every 25mg
aspartame) to achieve similar sweetness.

1

1

3498 - 3507

For six hours following consumption of the juice the number and
length of spike-wave bursts, indicative of an absence seizure, were
determined using EEG40 recordings. Each child was tested once with each
substance, on two consecutive days, treatments were assigned in a random
fashion. No information was provided regarding whether lunch or snacks were
given. There were no significant differences in either the frequency or
duration of spike-wave bursts; however, when the two factors were combined,
the total time spent in spike-wave per hour of observation was significantly
higher in children after consumption of aspartame compared with sucrose
(Camfield et al., 1992). The Panel noted that combination of the two factors
into a single measure was not adequately explained, and lack of control of
food and drink intake before and after dosing may have affected the results.

Page 696 Column 2

The number and length of spike-wave bursts, indicative of an
absence seizure, were determined using EEG40 recordings for 6 h following
consumption of the juice. Each child was tested once with each substance, on
two consecutive days, in random fashion. No information was provided
regarding whether lunch or snacks were given. There were no significant
differences in the frequency or duration of spike-wave bursts; however, when
the two factors were combined, the total time spent in spike-wave per
observation hour was significantly higher in children on the day aspartame
was consumed as compared to when sucrose was consumed (Camfield et al.,
1992). The major limitation of this study is the lack of control of food and
beverage intake before and after dosing with aspartame or sucrose because
fasting and dehydration can affect the susceptibility to seizures (Tollefson
and Barnard, 1992).

2

3

Notice at the end how the EFSA Panel always has something
negative to say about independent research that finds health problems caused
by aspartame. Also, notice that their negative information is sourced from
the aspartame manufacturer-funded review. For honest, scientific information
on aspartame and seizures, please see:
http://www.holisticmed.com/aspartame/abuse/seizures.html

3510 - 3513

Measurements prior to and following treatments included seizure
incidence, overall activity and behaviour, EEG recordings, adverse
experiences, liver function, urine analysis, and plasma levels of amino acid,
methanol, formate, glucose, and monoamines and metabolites. Children ate
their normal diet, but were asked to exclude a list of foods containing
aspartame.

Page 696 Column 2

Measurements prior to and following treatments included seizure
incidence, overall activity and behavior, EEG recordings, adverse
experiences, liver function, urine analysis, and plasma levels of amino acid,
methanol, formate, glucose, and monoamines and metabolites. Children were
allowed to eat their normal diet, but excluding foods on a list of
aspartame-containing products.

1

1

3518 - 3522

The subjects received placebo or 50 mg aspartame /kg bw in three
doses throughout the day, on days 2 and 4. EEG recordings were preformed for
five consecutive days. Meals were standardised throughout treatment. No
clinical seizures were observed in subjects during the study. Electrographic
seizures were recorded in two subjects on days consuming the placebo. Sleep
variables were also measured, but no effect of aspartame was observed.

Page 696 Column 2

In this study, subjects received 50 mg/kg bw aspartame or an
identical placebo in three divided doses throughout the day, on days 2 and 4.
EEG recordings were preformed for 5 consecutive days. All meals were
uniformly standardized on treatment days. No clinical seizures were observed
in subjects during the study. Electrographic seizures were recorded in 2
subjects on days consuming the placebo. Sleep variables were also measured,
but no effect of aspartame was observed.

4

2

The EFSA discussed manufacturer-sponsored "research"
related to aspartame and seizures, but neglected to mention that the subjects
were on anti-seizure medication during the short studies! They appear to be
too busy copying text to be bothered to actually read the research! For
honest, scientific information on aspartame and seizures, please see:
http://www.holisticmed.com/aspartame/abuse/seizures.html

3525 - 3528

The possible effect of aspartame on headaches has been
investigated in various studies, which reported conflicting results. Some
reported no effect and others suggested that a small subset of the population
may be susceptible to aspartame-induced headaches. The number of existing
studies was small, and several had high participant dropout rates, making
interpretation of results difficult.

Page 694 Column 1

Studies designed to evaluate the possible effect of aspartame on
headaches have reported conflicting results, with some reporting no effect
and others suggesting a small subset of the population may be susceptible to
aspartame-induced headaches. The number of studies is small and several have
high participant dropout rates, making interpretation of results difficult.

1

2

3529 - 3535

A double-blind crossover trial (Schiffman et al., 1987) with 40
individuals (12 males, 28 females; ages 19–69) who had previously reported
suffering headaches when they consumed aspartame, was a well controlled study
with patients being housed and monitored in an inpatient unit. Participants
were monitored for 2 days, and then challenged with capsules of aspartame (30
mg/kg bw) or placebo (microcrystalline cellulose) on days 3 and 5, with day 4
being a washout day. Diet and extraneous variables were controlled. There was
no evidence of an effect of aspartame, as incidence of headache after
consumption of aspartame (35%) or after the placebo (45%) was similar
(Schiffman et al., 1987).

Page 693 Column 1 and Column 2

A doubleblind crossover trial with 40 individuals (12 males, 28
females; ages 19–69) who had reported having headaches each time they
consumed aspartame was a well-controlled study with patients being housed and
monitored in an inpatient unit (Schiffman et al., 1987). Participants were
monitored for 2 days, and then challenged with capsules of aspartame (30
mg/kg bw) or placebo (microcrystalline cellulose) on days 3 and 5, with day 4
being a washout day. Diet and extraneous variables were controlled. There was
no evidence of an effect of aspartame, as incidence of headache after
consumption of aspartame (35%) was similar to after the placebo (45%)
(Schiffman et al., 1987).

3

1

The whole paragraph was plagiarized, even the phrase,
"well-controlled study!" Ha Ha! This one day study of aspartame was
designed in a way that no statistical difference would be seen For honest
scientific information on aspartame and headaches, please see:
http://www.holisticmed.com/aspartame/abuse/migraine.html

3536 - 3547

In contrast, the study by Koehler and Glaros (1988) had
volunteers who suffered with migraines and stayed in their normal
environments during a double-blind crossover study with three phases: a
4-week baseline phase and two four-week experimental phases, with a 1-week
washout phase betweentreatments.
Participants (two males, eight females; ages 18 to 47 years) consumed
capsules of aspartame (300 mg) or placebo (microcrystalline cellulose) and
self-recorded incidence of headaches and dietary information. The incidence
of headaches did not differ from baseline during the placebo phase. Five of
the eleven participants reported a higher number of migraines during the
aspartame phase compared to during the baseline or placebo phases. The mean
number of headaches reported was 1.72, 1.55, and 3.55 during the baseline,
placebo, and aspartame phases, respectively. No differences were reported in
the intensity or duration of migraine headaches. Dietary records did not show
any substantial changes in diet among phases. The high dropout rate, from 25
to 11 participants in this study makes interpretation of the results
difficult.

Page 693 Column 2

In contrast, the study by Koehler and Glaros (1988) had
volunteers who suffered with migraines stay in their normal environments
during a double-blind crossover study with three phases: a 4-week baseline
phase, two 4-week experimental phases, and a 1-week washout phase between
treatments. Participants (n =11; 2 males, 8 females; ages 18 to 47 years)
consumed capsules of aspartame (300 mg) or placebo (microcrystalline
cellulose) and self-recorded headaches and diets. The incidence of headaches
did not differ from baseline during the placebo phase. Five of the 11
participants reported a higher number of migraines during the aspartame phase
as compared to during the baseline or placebo phases. The mean number of
headaches reported was 1.72, 1.55, and 3.55 during the baseline, placebo, and
aspartame phases, respectively. No differences were reported in the intensity
or duration of migraine headaches. Dietary records did not show any
substantial changes in diet among phases. One concern is the small number of
individuals and high dropout rate from 25 down to 11 participants in this
study.

5

3

Independent study finds that aspartame can cause migraines. EFSA
lifts and rewords the criticism from the aspartame manufacturer review. For
honest scientific information on aspartame and headaches, please see:
http://www.holisticmed.com/aspartame/abuse/migraine.html

3548 - 3554

Patients at a headache unit were asked to complete a survey
reflecting whether they felt that alcohol, aspartame or carbohydrate intake
were triggers of headaches (Lipton et al., 1989). Of the 171 patients who
completed the survey, 8.3% reported aspartame as a trigger of headaches, and
often a migraine headache. As this was significantly higher than the response
to carbohydrates (2.3%), the authors concluded that aspartame might be a
migraine headache trigger for some individuals. The Panel considered ‘the
power of suggestion’ of having aspartame listed as a possible trigger of
headaches to be a major limitation of this study.

Page 693 Column 2

Patients at a headache unit (n = 190) were asked to complete a
survey regarding whether they felt that alcohol, aspartame or carbohydrate
intake were triggers of headaches (Lipton et al., 1989). The limitation of
this study is the power of suggestion by having aspartame listed as a
possible trigger and then asking for a response. Of the 171 patients who
completed the survey, 8.3% reported aspartame as a trigger of headaches, and
often a migraine headache. As this was significantly higher than the response
to carbohydrates (2.3%), the authors concluded that aspartame might be a
migraine headache trigger for some individuals.

3

1

The EFSA copies the paragraph and then rewords (and places in a
different location) the criticism from the aspartame manufacturer review. The
researchers had a control in the study to address the "power of
suggestion" criticism. For honest, scientific information about
headaches, please see:
http://www.holisticmed.com/aspartame/abuse/migraine.html

3555 - 3567

Van den Eeden et al. (1994) conducted a double-blind randomised
crossover trial with 32 subjects self-diagnosed as sensitive to aspartame.
Only 18 participants completed the full protocol, as other subjects withdrew
for various reasons including adverse effects. Subjects took capsules
containing either aspartame or placebo (microcrystalline cellulose) three
times a day to achieve a dose of 30 mg/kg bw/day for seven days. A
significantly higher (p = 0.04) occurrence of self-reported headaches was
recorded following exposure to aspartame (33% of days) compared to placebo
(24% of days). The subjects who had excess headaches following aspartame
dosing were those who had, at the beginning of the study, indicated they were
‘very sure’ that they were susceptible to aspartame-induced headaches. In
contrast, those subjects who classified themselves as ‘somewhat or not sure’
reported similar headache incidence during aspartame and placebo exposure
periods. The authors conclude that these results indicated that a small
subset of the population was susceptible to aspartame-induced headaches (Van
den Eeden et al., 1994). The Panel consider that with such a low number of
participants it was not possible to draw a conclusion.

Page 693 Column 2 - 694 Column 1

In the most recent study to assess whether the consumption of
aspartame is associated with headaches, Van den Eeden et al. (1994) conducted
a double-blind randomized crossover trial with 32 subjects who self-reported
sensitivity to aspartame. Only 18 participants completed the full protocol,
as other subjects withdrew for various reasons including adverse effects.
Subjects took capsules containing either aspartame or placebo
(microcrystalline cellulose) 3 times a day to achieve a dose of 30 mg/kg
bw/day for 7 days. A significantly higher (p = .04) occurrence of
self-reported headaches was reported following exposure to aspartame (33% of
days) as compared to placebo (24% of days). The subjects who had excess
headaches following aspartame dosing were those who had, at the beginning of
the study, indicated they were “very sure” that they were susceptible to
aspartame-induced headaches. In contrast, those subjects who classified
themselves as “somewhat or not sure” reported similar headache incidence during
aspartame and placebo exposure periods. The authors conclude that these
results indicate that a small subset of the population are susceptible to
aspartame-induced headaches (Van den Eeden et al., 1994).

6

1

The study authors did not conclude that "a small subset of
the population are susceptible to aspartame-induced headaches" as the
aspartame manufacturer-funded review claimed. The authors did not use the
term, "small." Amazingly, the EFSA criticized the study for the
small number of participants even though it had more participants than
aspartame manufacturer studies that they never criticize. For honest,
scientific information about headaches, please see:
http://www.holisticmed.com/aspartame/abuse/migraine.html

3570 - 3574

Drewnowski et al. (1994) fed 12 obese and 12 lean women one of
four breakfast preloads sweetened with 50 g sucrose or 500 mg aspartame, or
aspartame plus 50 g maltodextrin, in a cross-over design. As such all
subjects were tested with all treatments. Subsequent food intake and calorie
consumption during lunch, snack, and dinner was recorded and were reported
not to be affected by the sweetener consumed in the preload (Drewnowski et
al., 1994).

Page 697 Column 1

In one of the well-conducted studies, Drewnowski et al. (1994)
fed 12 obese and 12 lean women one of four breakfast preloads sweetened with
50 g sucrose, 500 mg aspartame, or aspartame plus 50 g maltodextrin. All
subjects were tested with all treatments. Subsequent food intake and calorie
consumption during lunch, snack, and dinner were not affected by the
sweetener consumed in the preload (Drewnowski et al., 1994).

1

2

At least the EFSA did not plagiarize "well-conducted
studies" as they did in line 3529 (see above).

3575-3580

A meta-analysis of 16 randomised controlled trials assessing the
effect of aspartame consumption on energy intake with observations on weight
loss and weight maintenance was undertaken by de la Hunty et al. (2006). The
studies that have addressed the question of the effect of aspartame on
appetite and body weight, that have actually measured food consumption, have
shown that aspartame does not increase caloric intake. Significant reduction
of energy intake with consumption of aspartame was observed, except when the
control was a non-sucrose control such as water (de la Hunty et al., 2006).

Page 697 Column 2

Recently, a meta-analysis of 16 randomized controlled trials
assessing the effect of aspartame consumption on weight loss, weight
maintenance and energy intake was conducted (de la Hunty et al., 2006). The
studies that have addressed the question of the effect of aspartame on
appetite and body weight, that have actually measured food consumption, have
shown that aspartame does not increase caloric intake. In contrast,
significant reduction of energy intake with consumption of aspartame compared
to other controls was observed, except when the control was a nonsucrose
control such as water.

This whole section appears to be lifted directly from the EFSA
"Report of the Meetings on Aspartame With National Experts (Question
Number: EFSA-Q-2009-00488) (2009) (Pages 26-27 and part from near the bottom
of page 48.) The EFSA appears to be plagiarizing material written by other
authors but published by EFSA. It might not be so bad except that on Pages
25-26 of their 2009 document they list the source material for their
discussion of aspartame and "allergies." The sources include one long
review written by the aspartame manufacturer (Butchko 2002), one long review
funded by the aspartame manufacturer (Magnuson 2007) and only two case
history reports. They did not include independent research and other
published case history reports. See the 2009 EFSA document at:
http://www.feingold.org/Research/PDFstudies/EFSAaspartame.pdf or
http://www.efsa.europa.eu/en/supporting/doc/1641.pdf

4987 - 4990

Olney and co-workers (Olney and Sharpe, 1969; Olney et al.,
1972) also reported neuronal necrosis in neonatal nonhuman primates
administered large bolus doses of glutamate (1000-4000 mg/kg bw
subcutaneously or orally. This observation, however, could not be reproduced
by a number of other scientists with either glutamate or aspartame at high
dosages (reviewed by Butchko et al., 2002).

See Notes section to the right.

Olney and co-workers (Olney and Sharpe, 1969; Olney et al.,
1972) also reported this phenomenon in neonatal nonhuman primates
administered large bolus doses of glutamate. This observation, however, could
not be reproduced by a number of other scientists with either glutamate or
aspartame at high dosages

1

1

This section was copied and pasted from page S26 of the
aspartame manufacturer review by Butchko (Reg Tox & Pharm, 35:S1-S93,
2002). If the EFSA had done event the slightest bit of reading about
aspartame, they would be aware that the industry research they are citing
involved giving brain-protecting drugs to the test animals in a study,
recropping a image from one species of monkey and putting it in another study
to represent another species, etc.